Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy
Open accessAbstract
This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple‐author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state‐of‐the‐art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society
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The effect of levodopa seems to decrease over years of use.
“in addition, its effect seems to decrease over the years (33).”
From A Review on Wearable Technologies for Tremor Suppression (2021) · cites this paper as [33]
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“More rapid progression of all clinical features was predicted by the presence of REM behavioral disorder, mild cognitive impairment, and orthostatic hypotension in another.(29) To date, PD subtypes have been characterized on the basis of readily apparent and evaluable clinical”
Self-citationProgressive parkinsonism in mice with respiratory-chain-deficient dopamine neurons
Ekstrand, M. I., Terzioglu, M., Galter, D., Zhu, S., Hofstetter, C., Lindqvist, E., Thams, S., Bergstrand, A., Hansson, F. S., Trifunovic, A., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605208103 · Cited by 605 · see citing works
MR-guided focused ultrasound thalamotomy for essential tremor: a proof-of-concept study
Lipsman, N., Schwartz, M. L., Huang, Y., Lee, L., Sankar, T., Chapman, M., Hynynen, K., & Lozano, A. M. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70048-6 · Cited by 604 · see citing works
Self-citationMarks, W. J., Ostrem, J. L., Verhagen, L., Starr, P. A., Larson, P. S., Bakay, R. A., Taylor, R., Cahn-Weiner, D. A., Stoessl, A. J., Olanow, C. W., et al. (2008) · The Lancet Neurology · doi:10.1016/s1474-4422(08)70065-6 · Cited by 596 · cited 1× · see citing works
“Although some open-label trials reported benefit,(282) a double-blind trial did not meet its primary endpoint.(283) Ceregene Inc.”
Self-citationUnderstanding Dopaminergic Cell Death Pathways in Parkinson Disease
Michel, P. P., Hirsch, É. C., & Hunot, S. (2016) · Neuron · doi:10.1016/j.neuron.2016.03.038 · Cited by 594 · cited 1× · see citing works
“The rapid advance in research techniques during the past 20 years has determined that there is not a single cause but several causes all leading to the common preferential early loss of dopaminergic neurons in the SN in patients with clinical PD.(68) The 2 most obvious culprits are the many different genes involved (a…”
Multiple hit hypotheses for dopamine neuron loss in Parkinson's disease
Sulzer, D. (2007) · Trends in Neurosciences · doi:10.1016/j.tins.2007.03.009 · Cited by 583 · cited 1× · see citing works
“SNc dopaminergic neurons also have the added liability of using dopamine as a neurotransmitter.(257) For example, the conjunction of dopamine, Ca(21) influx through plasma membrane Cav1 channels, and alphasynuclein disrupt chaperone mediated autophagy, promoting neurodegeneration.”
Mitochondria: The Next (Neurode)Generation
Schon, E. A., & Przedborski, S. (2011) · Neuron · doi:10.1016/j.neuron.2011.06.003 · Cited by 568 · cited 1× · see citing works
“Second is the case of PINK1 and Parkin mutations that in humans cause recessive forms of familial PD and in flies major defects of mitochondria.(85) These observations reinvigorated the discussion of mitochondria defect in PD pathogenesis, but this time no longer from the angle of a deficit in bioenergics that have be…”
Self-citationRaz, A., Vaadia, E., & Bergman, H. (2000) · Journal of Neuroscience · doi:10.1523/jneurosci.20-22-08559.2000 · Cited by 567 · cited 1× · see citing works
“In the past, theories of tremor genesis were focused on the idea that there are specific cell groups that have the tendency to oscillate and a mechanism that is related to the neurodegeneration synchronizes their oscillations.(202) However, it cannot be excluded that the oscillations are generated within brain network…”
Self-citationGlucocerebrosidase Deficiency in Substantia Nigra of Parkinson Disease Brains
Gegg, M. E., Burke, D., Heales, S., Cooper, J., Hardy, J., Wood, N., & Schapira, A. (2012) · Annals of Neurology · doi:10.1002/ana.23614 · Cited by 551 · see citing works
Self-citationNeurodegenerative Disorder Risk in Idiopathic REM Sleep Behavior Disorder: Study in 174 Patients
Iranzo, A., Fernández-Arcos, A., Tolosa, E., Serradell, M., Molinuevo, J. L., Valldeoriola, F., Gelpi, E., Vilaseca, I., Sánchez-Valle, R., Lladó, A., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0089741 · Cited by 548 · see citing works
Self-citationMosharov, E. V., Larsen, K. E., Kanter, E., Phillips, K. A., Wilson, K., Schmitz, Y., Krantz, D. E., Kobayashi, K., Edwards, R. H., & Sulzer, D. L. (2009) · Neuron · doi:10.1016/j.neuron.2009.01.033 · Cited by 530 · see citing works
Pont‐Sunyer, C., Hotter, A., Gaig, C., Seppi, K., Compta, Y., Katzenschlager, R., Mas, N., Hofeneder, D., Brücke, T., Bayés, A., et al. (2015) · Movement Disorders · doi:10.1002/mds.26077 · Cited by 511 · cited 1× · see citing works
“behavioral disorder, may even be the earliest disease manifestations, occurring years before any of the defining motor features are present.(19) Clearly, Parkin-”
Self-citationBerg, D., Postuma, R. B., Bloem, B. R., Chan, P., Dubois, B., Gasser, T., Goetz, C. G., Halliday, G. M., Hardy, J., Lang, A. E., et al. (2014) · Movement Disorders · doi:10.1002/mds.25844 · Cited by 505 · cited 1× · see citing works
“”(1) Even with today’s insights from genetics and pathology, defining PD remains a challenge.(164) Moreover,”
Self-citationIs alpha-synuclein in the colon a biomarker for premotor Parkinson’s disease? Evidence from 3 cases
Shannon, K. M., Keshavarzian, A., Dodiya, H. B., Jakate, S., & Kordower, J. H. (2012) · Movement Disorders · doi:10.1002/mds.25020 · Cited by 464 · cited 1× · see citing works
“Indeed, alphasynuclein accumulation in the periphery has been well described,(5) with some studies suggesting the presence of LP in the colon prior to the onset of the classic motor features of PD.(267) Misfolded proteins could also form stochastically in a random fashion and lead to the accumulation of aggregated pro…”
Self-citationA large kindred with autosomal dominant Parkinson's disease
Golbe, L., Iorio, G. D., Bonavita, V., Miller, D. C., & Duvoisin, R. (1990) · Annals of Neurology · doi:10.1002/ana.410270309 · Cited by 463 · cited 1× · see citing works
“At the same time, the evidence for genetic contributions was accumulating in the form of families with multiple affected members, including some families with pathologically proven Lewy-body PD that could be a familial disorder.(145) During the past 2 decades, genetic risk factors and causative genes have continued to…”
Svennilson, E., Torvik, A., Lowe, R., & Leksell, L. (1960) · Acta Psychiatrica Scandinavica · doi:10.1111/j.1600-0447.1960.tb07606.x · Cited by 451 · cited 1× · see citing works
“In 1992, Laitinen and colleagues(184) published a seminal paper on the reexamination of pallidotomy in the treatment of PD, which he had learned from Leksell 3 decades earlier.(185) The rediscovery and reintroduction of pallidotomy rekindled interest in surgery for PD fostered by a few studies in the MPTP monkey model…”
Neuropathology of sporadic Parkinson's disease: Evaluation and changes of concepts
Jellinger, K. A. (2011) · Movement Disorders · doi:10.1002/mds.23795 · Cited by 447 · see citing works
Imaging amyloid deposition in Lewy body diseases
Gomperts, S. N., Rentz, D. M., Moran, E., Becker, J. A., Locascio, J. J., Klunk, W. E., Mathis, C. A., Elmaleh, D. R., Shoup, T., Fischman, A. J., et al. (2008) · Neurology · doi:10.1212/01.wnl.0000326146.60732.d6 · Cited by 443 · cited 1× · see citing works
“The PET ligand (11)C-PIB, a neutral thioflavin-T analogue developed to image ß-amyloid plaques in dementia, has been employed to assess the prevalence of amyloid in PD patients.(124) Amyloid plaques can be detected with (11)C-PIB PET in a majority of dementia with Lewy-body cases, but only a minority of PDD or PD-MCI.”
Excessive daytime sleepiness and subsequent development of Parkinson disease
Abbott, R. D., Ross, G. W., White, L. R., Tanner, C. M., Masaki, K., Nelson, J. S., Curb, J. D., & Petrovitch, H. (2005) · Neurology · doi:10.1212/01.wnl.0000183056.89590.0d · Cited by 439 · cited 2× · see citing works
“found that excessive napping or somnolence doubled the risk of PD.(230,234) Lead time is uncertain, but it is easily screened.”
Self-citationThe spectrum of nonmotor symptoms in early Parkinson disease
Khoo, T. K., Yarnall, A. J., Duncan, G. W., Coleman, S. Y., O'Brien, J. T., Brooks, D. J., Barker, R. A., & Burn, D. J. (2013) · Neurology · doi:10.1212/wnl.0b013e31827deb74 · Cited by 430 · see citing works
Self-citationEnvironmental risk factors and Parkinson's disease: An umbrella review of meta-analyses
Bellou, V., Belbasis, L., Tzoulaki, I., Εvangelou, Ε., & Ioannidis, J. P. A. (2015) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2015.12.008 · Cited by 429 · see citing works
Neuropathology underlying clinical variability in patients with synucleinopathies
Halliday, G. M., Holton, J. L., Révész, T., & Dickson, D. W. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0852-9 · Cited by 426 · cited 2× · see citing works
“For example, the most robust (and reciprocal) innervation of the SNc is onto striatal spiny projection neurons, which do not manifest LP in PD.(72,88) The appearance of Lewy-like pathology in striatal grafts(255) is also at odds with a simple synaptic spreading model because there”
Self-citationCaligiore, D., Pezzulo, G., Baldassarre, G., Bostan, A. C., Strick, P. L., Doya, K., Helmich, R. C. G., Dirkx, M. F., Houk, J. C., Jörntell, H., et al. (2016) · The Cerebellum · doi:10.1007/s12311-016-0763-3 · Cited by 423 · cited 2× · see citing works
“Akineto-rigid and tremor-dominant forms of PD were associated with structural and functional changes predominating in the basal ganglia—cortical and cerebello-thalamocortical networks, respectively,(99) with tremor-related activity first arising in the internal part of the globus pallidus and propagating to the cerebe…”
Edison, P., Rowe, C. C., Rinne, J. O., Ng, S., Ahmed, I., Kemppainen, N. M., Villemagne, V. L., O'Keefe, G. J., Någren, K., Chaudhuri, К. R., et al. (2008) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2007.127878 · Cited by 422 · cited 2× · see citing works
“In frankly demented PD patients, FDG PET shows reduced absolute levels of glucose utilization that targets the posterior cingulate, parietal, and temporal association areas.121 This pattern is present to a lesser extent in PD-MCI.122 Although the pattern of glucose hypometabolism in demented PD patients resembles that…”
Self-citationParkinson's disease: The quintessential neuropsychiatric disorder
Weintraub, D. A., & Burn, D. J. (2011) · Movement Disorders · doi:10.1002/mds.23664 · Cited by 422 · cited 1× · see citing works
“The high prevalence of cognitive impairment and protean psychiatric complications has changed how we conceptualize PD.(47,48) This has manifested itself in the recently proposed revised clinical diagnostic criteria,(17,49) which allows for dementia to be a comorbid condition at the time of diagnosis.”
Self-citationFDG PET in the differential diagnosis of parkinsonian disorders
Eckert, T., Barnes, A., DHAWAN, V. M., Frucht, S. J., Gordon, M. F., Feigin, A., & Eidelberg, D. (2005) · NeuroImage · doi:10.1016/j.neuroimage.2005.03.012 · Cited by 418 · see citing works
Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor
Helmich, R. C., Janssen, M. J. R., Oyen, W. J. G., Bloem, B. R., & Toni, I. (2011) · Annals of Neurology · doi:10.1002/ana.22361 · Cited by 417 · cited 2× · see citing works
“Further activation studies using tremor intensity as a measure to correlate the blood-oxygen-level dependent effect on MRI have shown that tremor onset is best correlated with a network within the basal ganglia (switching on tremor), whereas the tremor severity (dimmer of tremor) is related to the cerebello-cortical n…”
Stokholm, M. G., Danielsen, E. H., Hamilton‐Dutoit, S. J., & Borghammer, P. (2016) · Annals of Neurology · doi:10.1002/ana.24648 · Cited by 415 · cited 1× · see citing works
“A recent Danish study examined gastrointestinal biopsy samples from a national database in patients who eventually developed PD.(238) They documented increased phosphorylated synuclein staining in those destined to develop PD; 45% of prodromal PD samples were positive (median interval 5 7 years before PD diagnosis), c…”
A controlled trial of antidepressants in patients with Parkinson disease and depression
Menza, M. A., Dobkin, R. D., Marín, H., Mark, M. H., Gara, M. A., Buyske, S. G., Bienfait, K., & Dicke, A. (2008) · Neurology · doi:10.1212/01.wnl.0000336340.89821.b3 · Cited by 413 · see citing works
Resting state functional connectivity of the striatum in Parkinson’s disease
Hacker, C. D., Perlmutter, J. S., Criswell, S. R., Ances, B. M., & Snyder, A. Z. (2012) · Brain · doi:10.1093/brain/aws281 · Cited by 405 · see citing works
de la Fuente‐Fernández, R. (2004) · Brain · doi:10.1093/brain/awh290 · Cited by 404 · see citing works
Self-citationMagnetic resonance imaging markers of Parkinson's disease nigrostriatal signature
Péran, P., Cherubini, A., Assogna, F., Piras, F., Quattrocchi, C., Peppe, A., Celsis, P., Rascol, O., Démonet, J.-F., Stefani, A., et al. (2010) · Brain · doi:10.1093/brain/awq212 · Cited by 399 · see citing works
Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion‐Like Disorder?
Olanow, C. W., & Brundin, P. (2013) · Movement Disorders · doi:10.1002/mds.25373 · Cited by 392 · cited 1× · see citing works
“Importantly, the prion hypothesis identifies a series of novel targets and candidate therapeutic interventions that might prevent the formation or facilitate the clearance of misfolded alpha-synuclein and thereby have disease-modifying effects.(268,269)”
Self-citationMetabolic brain networks in neurodegenerative disorders: a functional imaging approach
Eidelberg, D. (2009) · Trends in Neurosciences · doi:10.1016/j.tins.2009.06.003 · Cited by 389 · cited 4× · see citing works
“degree of expression correlates with the degree of motor disability.(107) The PDRP normalizes after successful treatment with both dopaminergic drugs or DBS.”
InfluentialAccuracy of clinical diagnosis of Parkinson disease: A systematic review and meta-analysis
Jellinger, K., Logroscino, G., Rizzo, G., Copetti, M., Arcuti, S., Martino, D., & Fontana, A. (2016) · Neurology · doi:10.1212/wnl.0000000000002876 · Cited by 384 · cited 2× · see citing works
“Imaging may be helpful, in particular if specific MRI changes precede satisfaction of clinical criteria,(42) but accuracy of diagnosis based on MRI findings and PET/single-photon emission computerized tomography (SPECT) imaging is not higher than clinical expertise in clinicopathological studies.(33) Drug-induced park…”
Respondek, G., Stamelou, M., Kurz, C., Ferguson, L. W., Rajput, A. H., Chiu, W. Z., Swieten, J. C. V., Troakes, C., Sarraj, S. A., Gelpí, E., et al. (2014) · Movement Disorders · doi:10.1002/mds.26054 · Cited by 384 · see citing works
Self-citationPenney, J., Oakes, D., Shoulson, I., Fahn, S., Lang, A., Langston, J., LeWitt, P., Olanow, C., Tanner, C., & Kieburtz, K. (1996) · Annals of Neurology · doi:10.1002/ana.410390107 · Cited by 380 · cited 1× · see citing works
“5 months of levodopa therapy half experienced a wearing-off phenomenon.(179) In the ELLDOPA study, 16.”
Self-citationHoltzman, R. M. (2013) · História, Ciências, Saúde: Manguinhos · doi:10.1590/s0104-59702013000500001 · Cited by 376
Snow, B., Tooyama, I., Mcgeer, E., Yamada, T., Calne, D., Takahashi, H., & Kimura, H. (1993) · Annals of Neurology · doi:10.1002/ana.410340304 · Cited by 367 · see citing works
Pooled analysis of tobacco use and risk of Parkinson disease.
Ritz, B., Ascherio, A., Checkoway, H., Marder, K., Nelson, L., Rocca, W., Ross, G., Strickland, D., den Eeden, S. K. V., & Gorell, J. (2007) · Archives of Neurology · doi:10.1001/archneur.64.7.990 · Cited by 366 · cited 2× · see citing works
“Smokeless tobacco users are also at lower risk of PD, indirectly supporting an effect of nicotine.(151) Variants in several genes have been reported to modify the effect of smok-”
Self-citationVitamin K 2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency
Vos, M. H., Esposito, G., Edirisinghe, J. N., Vilain, S., Haddad, D., Slabbaert, J. R., Meensel, S. V., Schaap, O., Strooper, B. D., Meganathan, R., et al. (2012) · Science · doi:10.1126/science.1218632 · Cited by 364 · cited 1× · see citing works
“Drosophila identified vitamin K2 as a suppressor of the PINK1 mutant phenotype, which functions as an electron carrier molecule in mitochondria leading to improved ATP production.(167) It has thus been hypothesized that stratifying PD patients according to different degrees of mitochondrial dysfunction based on their…”
Midbrain iron content in early Parkinson disease
Martin, W. R. W., Wieler, M., & Gee, M. (2008) · Neurology · doi:10.1212/01.wnl.0000286384.31050.b5 · Cited by 355 · cited 2× · see citing works
“Increased iron content may predominate in the lateral segments of the SN and in some studies correlated with the UPDRS motor score.(88) A number of studies have reported altered diffusion properties in the SN, characterized by reduced fractional anisotropy, but the large variability of the results question the reliabi…”
Postuma, R., Lang, A.-E., Gagnon, J., Pelletier, A., & Montplaisir, J. (2012) · Brain : a journal of neurology · doi:10.1093/brain/aws093 · Cited by 352 · cited 1× · see citing works
“Whereas redundancy is common in many neurodegenerative disorders, a unique advantage of PD is that it has a nonmotor prodrome.(221) Arguably one of the most important new insights during the past 20 years is that PD can start outside of the SNpc.”
Self-citationJellinger, K. A. (1999) · Journal of neural transmission. Supplementum · doi:10.1007/978-3-7091-6360-3_1 · Cited by 349 · cited 1× · see citing works
“One of the main claims of earlier papers was that the cells of the Area 8 close to the SN and caudal to the red nucleus are preferentially degenerating.(198,199) This is in keeping with the suggested differential pattern of degeneration between tremor-dominant patients and akinesiadominant patients.”
Dopamine Agonist Withdrawal Syndrome in Parkinson Disease
Rabinak, C. A., & Nirenberg, M. J. (2010) · Archives of Neurology · doi:10.1001/archneurol.2009.294 · Cited by 347 · cited 2× · see citing works
“Indeed, DBS is increasingly used as a treatment to address the problem of reducing dopaminergic drugs without inducing motor deterioration in patients with ICD.(62) Cognitive impairment (particularly impaired verbal fluency) post-DBS surgery has consistently been reported, with some evidence that these effects are pre…”
A randomized, double-blind, placebo-controlled trial of antidepressants in Parkinson disease
Richard, I., McDermott, M. P., Kurlan, R., Lyness, J. M., Como, P. G., Pearson, N., Factor, S. A., Juncos, J. L., Ramos, C. S., Brodsky, M., et al. (2012) · Neurology · doi:10.1212/wnl.0b013e3182516244 · Cited by 336 · see citing works
Complex I and Parkinson's Disease
Greenamyre, J. T., Sherer, T., Betarbet, R. S., & Panov, A. V. (2001) · IUBMB Life · doi:10.1080/15216540152845939 · Cited by 335 · cited 2× · see citing works
“drial electron transport chain) is diminished in the SN, suggesting mitochondrial damage.(247) Third, in PD”
Nonmotor features of Parkinson's disease subtypes
Marras, C., & Chaudhuri, К. R. (2016) · Movement Disorders · doi:10.1002/mds.26510 · Cited by 327 · see citing works
Self-citationExposure to pesticides or solvents and risk of Parkinson disease
Pezzoli, G., & Cereda, E. (2013) · Neurology · doi:10.1212/wnl.0b013e318294b3c8 · Cited by 327 · see citing works
Use of ibuprofen and risk of Parkinson disease
Gao, X., Chen, H., Schwarzschild, M. A., & Ascherio, A. (2011) · Neurology · doi:10.1212/wnl.0b013e31820f2d79 · Cited by 323 · see citing works
Games, D., Valera, E., Spencer, B. J., Rockenstein, E. M., Mante, M., Adame, A., Patrick, C., Ubhi, K. K., Nuber, S., Sacayon, P., et al. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.5314-13.2014 · Cited by 322 · see citing works
Iranzo, Á., Valldeoriola, F., Lomeña, F., Molinuevo, J., Serradell, M., Salamero, M., Cot, A., Ros, D., Pavía, J., Santamaria, J., et al. (2011) · Lancet Neurology · doi:10.1016/s1474-4422(11)70152-1 · Cited by 319 · see citing works
Self-citationMcNeill, A., Magalhães, J., Shen, C.-G., Chau, K., Hughes, D., Mehta, A., Foltynie, T., Cooper, J., Abramov, A., Gegg, M. E., et al. (2014) · Brain : a journal of neurology · doi:10.1093/brain/awu020 · Cited by 315 · see citing works
Self-citationDopamine Is Required for the Neural Representation and Control of Movement Vigor
Panigrahi, B., Martin, K. A., Li, Y., Graves, A. R., Vollmer, A., Olson, L., Mensh, B. D., Karpova, A. Y., & Dudman, J. T. (2015) · Cell · doi:10.1016/j.cell.2015.08.014 · Cited by 315 · cited 1× · see citing works
“The dramatic and immediate beneficial effects of ablation and DBS of GPi in both primate models and patients with PD and dystonia, with little or no impairment of movement or behavior, argues against an essential role of the basal ganglia in the on-line control of movement and favors the view, now strongly supported b…”
García-Lorenzo, D., Santos, C. L.-D., Ewenczyk, C., Leu‐Semenescu, S., Galléa, C., Quattrocchi, G., Lobo, P. P., Poupon, C., Benali, H., Arnulf, I., et al. (2013) · Brain · doi:10.1093/brain/awt152 · Cited by 314 · see citing works
Neumann, W., Degen, K., Schneider, G., Brücke, C., Huebl, J., Brown, P., & Kühn, A. (2016) · Movement Disorders · doi:10.1002/mds.26759 · Cited by 312 · see citing works
Pathophysiology of Parkinson's disease: From clinical neurology to basic neuroscience and back
Bergman, H., & Deuschl, G. (2002) · Movement Disorders · doi:10.1002/mds.10140 · Cited by 310 · cited 1× · see citing works
“Several hypotheses have been put forward.(205,206) The first suggestion is the thalamic oscillator hypothesis assuming that thalamic cells oscillate and drive PD tremor, probably through the motor cortex.”
Self-citationCognitive-Behavioral Therapy for Depression in Parkinson's Disease: A Randomized, Controlled Trial
Dobkin, R. D., Menza, M., Allen, L. A., Gara, M. A., Mark, M. H., Tiu, J., Bienfait, K. L., & Friedman, J. (2011) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2011.10111669 · Cited by 310 · cited 1× · see citing works
“In addition, cognitive behavior therapy has been shown to be efficacious,(5) but its role in the management of cognitive impairment in PD is not yet cleart.(56) Among the disorders of affect, both anxiety and apathy in PD have received less attention than depression despite their frequent occurrence (30%-40% for each…”
Lectures on the diseases of the nervous system, delivered at La Salpêtrière, 2nd ed.
Charcot, J., & Sigerson, G. (n.d.) · doi:10.1037/12839-000 · Cited by 309
Hall, H., Reyes, S., Landeck, N., Bye, C. R., Leanza, G., Double, K. L., Thompson, L. H., Halliday, G. M., & Kirik, D. (2014) · Brain · doi:10.1093/brain/awu193 · Cited by 306 · cited 1× · see citing works
“However, the pattern of dopamine cell loss in the SN is distinctive for PD, with the most severe loss found in the ventrolateral region of the SN, whereas dopaminergic neurons in the nearby ventral tegmental area are nearly entirely spared.(65) Moderate to severe loss of the pigmented dopamine neurons in the SN is fou…”
Self-citationA critical appraisal of the pathogenic protein spread hypothesis of neurodegeneration
Walsh, D. M., & Selkoe, D. J. (2016) · Nature reviews. Neuroscience · doi:10.1038/nrn.2016.13 · Cited by 290 · cited 1× · see citing works
“Although cell-to-cell transmission of alpha-synuclein has been demonstrated in both cell culture and animal models, the exact sequence and molecular mechanisms of propagation of PD’s neuropathology throughout the human brain remain elusive.(157) PARK-LRRK2.”
Olanow, C. W., Bartus, R. T., Baumann, T. L., Factor, S. A., Boulis, N. M., Stacy, M. A., Turner, D. A., Marks, W. J., Larson, P., Starr, P. A., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24436 · Cited by 287 · cited 1× · see citing works
“However, multiple clinical trials, including 2 phase II trials, failed to meet the primary endpoint.(284) Uncertainty remains about the potential efficacy of trophic factors in PD.”
Self-citationAdams, J. R., van Netten, H., Schulzer, M., Mak, E., McKenzie, J., Strongosky, A., Sossi, V., Ruth, T. J., Lee, C. S., Farrer, M., et al. (2005) · Brain : a journal of neurology · doi:10.1093/brain/awh607 · Cited by 270 · see citing works
Self-citationClinical spectrum of levodopa‐induced complications
Aquino, C., & Fox, S. H. (2014) · Movement Disorders · doi:10.1002/mds.26125 · Cited by 269 · cited 1× · see citing works
“Motor complications (ie, fluctuations and dyskinesias) associated with chronic levodopa therapy represent a major challenge in the treatment of patients with PD.(177,178) In a large, prospective study, 29% of 352 patients originally enrolled in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP…”
Diógenes, M. J., Dias, R. B., Rombo, D. M., Miranda, H. V., Maiolino, F., Guerreiro, P. S., Näsström, T., Franquelim, H. G., Oliveira, L. M. A., Castanho, M. A. R. B., et al. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.0234-12.2012 · Cited by 268 · see citing works
Autophagy and A lpha‐ S ynuclein: R elevance to P arkinson's D isease and R elated S ynucleopathies
Xilouri, M., Brekk, O. R., & Stefanis, L. (2016) · Movement Disorders · doi:10.1002/mds.26477 · Cited by 266 · cited 1× · see citing works
“Genetic mutations affecting both have been implicated in PD.(245,246)”
A new dynamic model of the cortico-basal ganglia loop
Nambu, A. (2004) · Progress in brain research · doi:10.1016/s0079-6123(03)43043-4 · Cited by 263 · cited 1× · see citing works
“The STN also receives input from the cortex, the “hyperdirect” pathway, which is postulated to play a role in the cancellation of an inappropriate movement.(141) It is likely that other structures and feedback loops, such as those involving the pedunculopontine nucleus (PPN) and the Centromedianum (CM) also contribute…”
Nandhagopal, R., Kuramoto, L., Schulzer, M., Mak, E., Cragg, J. J., Lee, C. S., McKenzie, J., McCormick, S., Samii, A., Troiano, A. R., et al. (2009) · Brain · doi:10.1093/brain/awp209 · Cited by 262 · cited 1× · see citing works
“in early (or presumably presymptomatic) phases of disease.(112) Reverse extrapolation of the exponential defining this pattern of decline suggests that vesicular monoamine transporter type 2 binding declines first (more than 15 years prior to disease onset), followed by a decline in DAT binding (some 10-15 years prior…”
Self-citationMure, H., Hirano, S., Tang, C. C., Isaias, I. U., Antonini, A., Ma, Y., DHAWAN, V. M., & Eidelberg, D. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2010.09.028 · Cited by 259 · see citing works
Disease‐modifying strategies for Parkinson's disease
Kalia, L. V., Kalia, S. K., & Lang, A. E. (2015) · Movement Disorders · doi:10.1002/mds.26354 · Cited by 254 · cited 1× · see citing works
“lnflammation is a major component of PD pathogenesis, and a clinical trial using Pioglitazone, a peroxisome proliferator-activated receptor-g agonist that reduces proinflammatory cytokines and modulates mitochondrial biogenesis, was performed.(70,273) However, this trial failed to meet its primary endpoint as well.”
Self-citationLevodopa‐induced dyskinesias in Parkinson's disease: Clinical and pharmacological classification
Luquin, M., Scipioni, O., Vaamonde, J., Gershanik, O., & Obeso, J. (1992) · Movement Disorders · doi:10.1002/mds.870070204 · Cited by 246 · cited 2× · see citing works
“It is typically manifested by the onset of unilateral leg stereotypy followed by other abnormal involuntary movements involving the ipsilateral and then contralateral body within 10 to 15 minutes after ingesting levodopa, lasting about 15 minutes, after which time there is improvement of parkinsonism for several hours…”
Self-citationSerotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson’s disease patients
Politis, M., Wu, K., Loane, C., Brooks, D. J., Kiferle, L., Turkheimer, F., Bain, P. G., Molloy, S., & Piccini, P. P. (2014) · Journal of Clinical Investigation · doi:10.1172/jci71640 · Cited by 245 · cited 1× · see citing works
“Levodopa-induced dyskinesias thus likely reflect an aberrant pattern of dopamine release; this may arise from conversion of levodopa to dopamine in surviving serotonergic neurons, as suggested in animal models and supported by imaging studies.(116) Dyskinesias have also been linked to reduced opioid receptor,(117) inc…”
Self-citationAsymmetric pedunculopontine network connectivity in parkinsonian patients with freezing of gait
Fling, B. W., Cohen, R. G., Mancini, M., Nutt, J. G., Fair, D. A., & Horak, F. B. (2013) · Brain · doi:10.1093/brain/awt172 · Cited by 244 · see citing works
The thalamostriatal system in normal and diseased states
Smith, Y., Galván, A., Ellender, T. J., Doig, N. M., Villalba, R. M., Huerta-Ocampo, I., Wichmann, T., & Bolam, J. P. (2014) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2014.00005 · Cited by 244 · cited 1× · see citing works
“In addition, the CMstriatal projection has been found to degenerate in PD patients.(142) In parkinsonian animals, lesioning of the PPN, which may include the brainstem locomotor region, has been associated with akinesia, whereas increased PPN activity is associated with an amelioration of parkinsonism.”
Patterns and stages of α-synucleinopathy
ZACCAI, J. H., Brayne, C., McKeith, I. G., Matthews, F. E., & Ince, P. G. (2008) · Neurology · doi:10.1212/01.wnl.0000306697.48738.b6 · Cited by 244 · see citing works
Inosine to Increase Serum and Cerebrospinal Fluid Urate in Parkinson Disease
Schwarzschild, M. A., Ascherio, A., Beal, M. F., Cudkowicz, M., Curhan, G. C., Hare, J. M., Hooper, D. C., Kieburtz, K. D., Macklin, E. A., Oakes, D., et al. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2013.5528 · Cited by 244 · see citing works
Self-citationPostuma, R. B., Gagnon, J., Vendette, M., Desjardins, C., & Montplaisir, J. Y. (2010) · Annals of Neurology · doi:10.1002/ana.22282 · Cited by 242 · see citing works
Self-citationMinor hallucinations occur in drug‐naive Parkinson's disease patients, even from the premotor phase
Pagonabarraga, J., Martinez‐Horta, S., Fernández de Bobadilla, R., Pérez, J., Ribosa‐Nogué, R., Marín, J., Pascual‐Sedano, B., García, C., Gironell, A., & Kulisevsky, J. (2016) · Movement Disorders · doi:10.1002/mds.26432 · Cited by 236 · cited 1× · see citing works
“A recent study reported that the latter are common even in newly diagnosed, untreated patients.(58) Hallucinations were once thought to be almost exclusively visual, but auditory, tactile, and olfactory hallucinations are also relatively common.”
Calcium, Bioenergetics, and Neuronal Vulnerability in Parkinson's Disease
Surmeier, D. J., & Schumacker, P. T. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.r112.410530 · Cited by 233 · cited 1× · see citing works
“The following 3 uncommon traits are shared by the small collection of neurons at risk in PD: long, highly branched axons with many alphasynuclein enriched vesicular release sites; autonomous pacemaking activity that triggers a pronounced elevation in cytosolic Ca(21) concentration; and high basal mitochondrial oxidant…”
Self-citationCerebral Glucose Metabolic Features of Parkinson Disease and Incident Dementia: Longitudinal Study
Bohnen, N., Koeppe, R., Minoshima, S., Giordani, B., Albin, R., Frey, K., & Kuhl, D. (2011) · Journal of Nuclear Medicine · doi:10.2967/jnumed.111.089946 · Cited by 229 · cited 2× · see citing works
“Cholinergic terminal function in PD has been assessed with (11)C-NMP4A and (11)C-PMP PET, markers of acetylcholine esterase activity.(123,127) Nondemented PD patients showed posteriorly reduced cholinergic function in parietal and occipital cortex with (11)C-NMP4A PET, and this spreads to involve frontal cortex when d…”
Depressive symptoms in PD correlate with higher 5-HTT binding in raphe and limbic structures
Politis, M., Wu, K., Loane, C., Turkheimer, F., Molloy, S., Brooks, D. J., & Piccini, P. P. (2010) · Neurology · doi:10.1212/wnl.0b013e3181feb2ab · Cited by 224 · see citing works
Self-citationKalaitzakis, M. E., Graeber, M. B., Gentleman, S., & Pearce, R. K. B. (2007) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2007.00923.x · Cited by 224 · cited 1× · see citing works
“First, although all PD brains manifest LP in a stereotyped collection of nuclei, there are many deviations from the original staging model of Braak and colleagues, arguing against a stereotyped spread of LP through the brain.(252,253) Second, the distribution of LP in PD does not conform to a simple connectome rule.”
Rodríguez‐Oroz, M., López‐Azcárate, J., García‐García, D., Alegre, M., Toledo, J. B., Valencia, M., Guridi, J., Artieda, J., & Obeso, J. A. (2010) · Brain · doi:10.1093/brain/awq301 · Cited by 223 · cited 2× · see citing works
“In PD patients who develop levodopa–induced dyskynesias (LIDs) and/or pathological impulsivity, a peak in the theta band is recorded in the STN.139 Although still controversial, it is widely believed that abnormal beta band synchrony and STN motor cortex coupling play a critical and important role in the production of…”
Self-citationAge‐specific progression of nigrostriatal dysfunction in Parkinson's disease
de la Fuente‐Fernández, R., Schulzer, M., Kuramoto, L., Cragg, J., Ramachandiran, N., Au, W. L., Mak, E., McKenzie, J., McCormick, S., Sossi, V., et al. (2011) · Annals of Neurology · doi:10.1002/ana.22284 · Cited by 222 · see citing works
Self-citationLongitudinal changes in free-water within the substantia nigra of Parkinson’s disease
Ofori, E., Pasternak, O., Planetta, P. J., Li, H., Burciu, R. G., Snyder, A. F., Lai, S., Okun, M. S., & Vaillancourt, D. E. (2015) · Brain · doi:10.1093/brain/awv136 · Cited by 222 · cited 1× · see citing works
“For instance, new metrics allowing the characterization of neurite orientation dispersion and density or free water may be more sensitive to PD pathology in the nigra.(90) Reduced connectivity of the SN with the basal ganglia and thalamus were also evidenced in PD patients using tractography-based methods and resting…”
Clinical correlates of raphe serotonergic dysfunction in early Parkinson's disease.
Qamhawi, Z., Towey, D., Shah, B., Pagano, G., Seibyl, J., Marek, K., Borghammer, P., Brooks, D., & Pavese, N. (2015) · Brain : a journal of neurology · doi:10.1093/brain/awv215 · Cited by 216 · cited 1× · see citing works
“This has now been confirmed with (123)I-FP-CIT SPECT in a large group of de novo patients.(197) Interestingly, the raphe serotonin transporter availability was inversely correlated with rest tremor severity, and tremulous PD had less raphe serotonin transporter density but less severe striatal dopaminergic deficits th…”
Self-citationClinical correlates of levodopa-induced dopamine release in Parkinson disease
Pavese, N., Evans, A., Tai, Y. F., Hotton, G. R., Brooks, D., Lees, A., & Piccini, P. (2006) · Neurology · doi:10.1212/01.wnl.0000242888.30755.5d · Cited by 201 · see citing works
Self-citationEsposito, F., Tessitore, A., Giordano, A., Micco, R. D., Paccone, A., Conforti, R., Pignataro, G., Annunziato, L., & Tedeschi, G. (2013) · Brain · doi:10.1093/brain/awt007 · Cited by 201 · see citing works
Patterns of levodopa response in Parkinson's disease: a clinico-pathological study.
Kempster, P., Williams, D. R., Selikhova, M., Holton, J., Révész, T., & Lees, A. J. (2007) · Brain : a journal of neurology · doi:10.1093/brain/awm142 · Cited by 198 · see citing works
Toward a redefinition of Parkinson's disease
Stern, M. B., Lang, A. E., & Poewe, W. H. (2012) · Movement Disorders · doi:10.1002/mds.24051 · Cited by 195 · see citing works
Self-citationSeven‐tesla magnetic resonance images of the substantia nigra in Parkinson disease
Kwon, D.-H., Kim, J.-M., Oh, S., Jeong, H., Park, S.-Y., Oh, E., Chi, J.-G., Kim, Y.-B., Jeon, B., & Cho, Z. (2012) · Annals of Neurology · doi:10.1002/ana.22592 · Cited by 192 · cited 2×
“This sign (called the dorsal nigral hyperintensity or DNH sign) has a diagnostic accuracy of more than 90%.(92) The second technique relies on the paramagnetic properties of neuromelanin, a pigment that is contained in the SN pars compacta (SNc).”
Depression and subsequent risk of Parkinson disease
Gustafsson, H., Nordström, A., & Nordström, P. (2015) · Neurology · doi:10.1212/wnl.0000000000001684 · Cited by 187 · see citing works
Erro, R., Vitale, C., Amboni, M., Picillo, M., Moccia, M., Longo, K., Santangelo, G., Rosa, A. D., Allocca, R., Giordano, F., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0070244 · Cited by 185 · cited 1× · see citing works
“Early urinary dysfunction characterized a “nonmotor dominant” subgroup and suggested a more malignant course in one study.(28) More rapid progression of all clinical features was predicted by the presence of REM behavioral disorder, mild cognitive impairment, and orthostatic hypotension in another.”
Environmental Toxins and Parkinson's Disease
Ratner, M. H., & Feldman, R. (2005) · doi:10.1201/9780203508596.sec2 · Cited by 185 · cited 3×
“In some cases, the adverse effect of a pesticide is increased in persons with genetically determined altered function of toxicant handling.(148) Conversely, other behaviors appear to protect against the adverse effects of pesticide exposure.”
Caffeine and risk of Parkinson’s disease in a large cohort of men and women
Palacios, N., Gao, X., McCullough, M. L., Schwarzschild, M. A., Shah, R., Gapstur, S., & Ascherio, A. (2012) · Movement Disorders · doi:10.1002/mds.25076 · Cited by 185 · cited 2× · see citing works
“Coffee and tea drinking as well as caffeine consumption are also associated with a lower risk of PD.(153)”
Why have we failed to achieve neuroprotection in Parkinson's disease?
Olanow, C. W., Kieburtz, K. D., & Schapira, A. H. V. (2009) · Annals of Neurology · doi:10.1002/ana.21461 · Cited by 184 · cited 1× · see citing works
“However, there remain many obstacles both to identifying therapies capable of modifying the natural course of PD and to testing their efficacy in clinical trials.(295) Using a combination of therapies targeting multiple pathogenetic pathways simultaneously offers some attraction.”
Self-citationPiccini, P., Weeks, R., & Brooks, D. (1997) · Annals of Neurology · doi:10.1002/ana.410420508 · Cited by 183 · see citing works
Self-citationPrecision medicine for disease modification in Parkinson disease
Espay, A. J., Brundin, P., & Lang, A. E. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2016.196 · Cited by 180 · cited 1× · see citing works
“An important active research goal is to define methods of distinguishing subtypes at the earliest stages of the disease with future expectation that advances in precision medicine will allow the application of patient subtype-specific disease modification strategies.(32) The differential diagnosis of PD is relevant fo…”
Self-citationPramipexole in patients with early Parkinson's disease (PROUD): a randomised delayed-start trial
Schapira, A., McDermott, M., Barone, P., Comella, C., Albrecht, S., Hsu, H., Massey, D., Mizuno, Y., Poewe, W., Rascol, O., et al. (2013) · Lancet Neurology · doi:10.1016/s1474-4422(13)70117-0 · Cited by 179 · cited 1× · see citing works
“Other trials(70) used imaging techniques to assess neuroprotection as the primary endpoint as opposed to clinical disease modification, and although initial studies suggested that pramipexole (CALM-PD) and ropinirole (REAL-PD) studies slowed the loss of dopamine imaging markers relative to levodopa, these changes are…”
Self-citationVilas, D., Iranzo, Á., TOLOSA, E. S., Aldecoa, I., Berenguer, J., Vilaseca, I., Martí, C. D., Serradell, M., Lomeña, F., Alós, L., et al. (2016) · The Lancet Neurology · doi:10.1016/s1474-4422(16)00080-6 · Cited by 177 · cited 1× · see citing works
“A recent study in idiopathic RBD found synuclein deposition in 8/9 submandibular gland samples (compared to none in controls).(239) If specificity issues can be resolved, there is considerable future promise for tissue biopsy in early detection of PD.”
Self-citationFunctional connectivity in the basal ganglia network differentiates PD patients from controls
Szewczyk-krolikowski, K., Menke, R., Rolinski, M., Duff, E., Salimi-Khorshidi, G., Filippini, N., Zamboni, G., Hu, M., & Mackay, C. (2014) · Neurology · doi:10.1212/wnl.0000000000000592 · Cited by 175 · see citing works
Eggers, C., Kahraman, D., Fink, G., Schmidt, M. C., & Timmermann, L. (2011) · Movement Disorders · doi:10.1002/mds.23468 · Cited by 175 · see citing works
Lysosomal Dysfunction and α‐Synuclein Aggregation in Parkinson's Disease: Diagnostic Links
Moors, T. E., Paciotti, S., Chiasserini, D., Calabresi, P., Parnetti, L., Beccari, T., & van de Berg, W. D. J. (2016) · Movement Disorders · doi:10.1002/mds.26562 · Cited by 175 · cited 1× · see citing works
“Genetic mutations affecting both have been implicated in PD.(245,246)”
Self-citationScience, medicine, and the future: Parkinson's disease.
Schapira, A. (1999) · British medical journal · doi:10.1136/bmj.318.7179.311 · Cited by 174 · cited 1× · see citing works
“A third term, neurorescue, may be used when an intervention targets the adverse pathogenetic pathways directly and is capable not only of protecting neurons but also restoring their diminished function.(270) Medicine as practiced in the time of James Parkinson had no access to cures, although reference was often made…”
Self-citationLigation of the anterior choroidal artery for involuntary movements-parkinsonism
Cooper, I. S. (1953) · Psychiatric quarterly · doi:10.1007/bf01562492 · Cited by 171 · cited 1× · see citing works
“Surgery was aborted and the patient awoke with no deficits and with clear clinical benefit on the basis of the resulting ischemic lesion of the subthalamic nucleus, the globus pallidus, and their projections.(182) This led to a flurry of arterial ligation surgeries, but the variability and unpredictability of outcomes…”
Meyers, R., Fry, W., Fry, F. J., Dreyer, L. L., Schultz, D. F., & Noyes, R. F. (1959) · Journal of Neurosurgery · doi:10.3171/jns.1959.16.1.0032 · Cited by 167 · see citing works
Automated Neuromelanin Imaging as a Diagnostic Biomarker for Parkinson's Disease
Castellanos, G., Fernández-Seara, M., Lorenzo-Betancor, O., Ortega-Cubero, S., Puigvert, M., Uranga, J., Vidorreta, M., Irigoyen, J., Lorenzo, E., Muñoz-Barrutia, A., et al. (2015) · Movement Disorders · doi:10.1002/mds.26201 · Cited by 164 · cited 1× · see citing works
“sitive to neuromelanin and show the SNpc as an area of high signal intensity.(93) Reduced size and signal”
Adenosine 2A receptor availability in dyskinetic and nondyskinetic patients with Parkinson disease
Ramlackhansingh, A., Bose, S., Ahmed, I., Turkheimer, F., Pavese, N., & Brooks, D. (2011) · Neurology · doi:10.1212/wnl.0b013e31821ccce4 · Cited by 164 · see citing works
Self-citationSequencing analysis of the ITPR1 gene in a pure autosomal dominant spinocerebellar ataxia series
van de Leemput, J., Vrièze, F. W.-D., Rafferty, I., Brás, J., Giunti, P., Fisher, E., Hardy, J. A., Singleton, A., & Houlden, H. (2010) · Movement Disorders · doi:10.1002/mds.22646 · Cited by 163 · see citing works
Lewy pathology is not the first sign of degeneration in vulnerable neurons in Parkinson disease
Milber, J. M., Noorigian, J. V., Morley, J. F., Petrovitch, H., White, L., Ross, G. W., & Duda, J. E. (2012) · Neurology · doi:10.1212/wnl.0b013e318278fe32 · Cited by 163 · see citing works
Self-citationThe medical treatment of Parkinson disease from James Parkinson to George Cotzias
Fahn, S. (2014) · Movement Disorders · doi:10.1002/mds.26102 · Cited by 162 · cited 1× · see citing works
“dopamine in the brain and the second by Oleh Hornykiewicz, who demonstrated that the largest group of dopaminergic neurons are found in the SN with their terminals in the caudate nucleus.(64) The degeneration of the dopaminergic pigmented neurons in the SN is the most consistent neuropathological feature found in all…”
Self-citationα-Synuclein-Based Animal Models of Parkinson's Disease: Challenges and Opportunities in a New Era
Visanji, N. P., Brotchie, J. M., Kalia, L. V., Koprich, J. B., Tandon, A., Watts, J. C., & Lang, A. E. (2016) · Trends in Neurosciences · doi:10.1016/j.tins.2016.09.003 · Cited by 161 · see citing works
Self-citationFunctional connectivity and cognitive decline over 3 years in Parkinson disease
Dubbelink, K. T. E. O., Schoonheim, M. M., Deijen, J. B., Twisk, J. W. R., Barkhof, F., & Berendse, H. W. (2014) · Neurology · doi:10.1212/wnl.0000000000001020 · Cited by 160 · cited 1× · see citing works
“Changes in functional connectivity in anterior brain regions seemed to be related to executive dysfunction, whereas changes in more posterior regions may be related to the evolution to dementia.(104) Cognitive heterogeneity in PD may be mediated through common genetic variation of several genes including catechol-o-me…”
Schwarz, S., Abaei, M., Gontu, V., Morgan, P., Bajaj, N., & Auer, D. (2013) · NeuroImage: Clinical · doi:10.1016/j.nicl.2013.10.006 · Cited by 159 · see citing works
Changing the research criteria for the diagnosis of Parkinson's disease: obstacles and opportunities
Berg, D., Lang, A. E., Postuma, R. B., Maetzler, W., Deuschl, G., Gasser, T., Siderowf, A. D., Schapira, A. H. V., Oertel, W. H., Obeso, J. A., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70047-4 · Cited by 158 · see citing works
Self-citationα-Synuclein Suppression by Targeted Small Interfering RNA in the Primate Substantia Nigra
McCormack, A. L., Mak, S. K., Henderson, J. M., Bumcrot, D. A., Farrer, M. J., & Monte, D. A. D. (2010) · PLoS ONE · doi:10.1371/journal.pone.0012122 · Cited by 158 · cited 1× · see citing works
“More exciting are attempts to disaggregate aggregated synuclein, facilitate its clearance by augmenting autophagy pathways, or using antibodies to prevent its propagation from the periphery to the brain and once in the brain across the neuraxis.(288) Farthest along are vaccines against alphasynuclein as both active an…”
Biomarkers for dementia and mild cognitive impairment in Parkinson's disease
Delgado‐Alvarado, M., Gago, B., Navalpotro‐Gómez, I., Jiménez‐Urbieta, H., & Rodríguez‐Oroz, M. (2016) · Movement Disorders · doi:10.1002/mds.26662 · Cited by 158 · cited 1× · see citing works
“PD with dementia when compared with PD-MCI and accelerates with disease progression.(102,103) Changes in functional connectivity in anterior brain regions seemed to be related to executive dysfunction, whereas changes in more posterior regions may be related to the evolution to dementia.”
Mild cognitive impairment as a risk factor for Parkinson's disease dementia
Hoogland, J., Boel, J. A., de Bie, R. M. A., Geskus, R. B., Schmand, B. A., Dalrymple‐Alford, J. C., Marras, C., Adler, C. H., Goldman, J. G., Tröster, A. I., et al. (2017) · Movement Disorders · doi:10.1002/mds.27002 · Cited by 158 · see citing works
Self-citationPatterns of bursting occurring in thalamic cells during parkinsonian tremor.
Zirh, T., Lenz, F., Reich, S., & Dougherty, P. (1998) · Neuroscience · doi:10.1016/s0306-4522(97)00295-9 · Cited by 155 · see citing works
Lessons from the rotenone model of Parkinson’s disease
Greenamyre, J., Cannon, J. R., Drolet, R., & Mastroberardino, P. (2010) · TIPS - Trends in Pharmacological Sciences · doi:10.1016/j.tips.2009.12.006 · Cited by 154 · cited 1× · see citing works
“another environmental toxin associated with PD, also is a mitochondrial poison.(247,248) Second, in PD brains,”
Parkin Disease: A Clinicopathologic Entity?
Doherty, K., Silveira-Moriyama, L., Parkkinen, L., Healy, D., Farrell, M., Mencacci, N., Ahmed, Z., Brett, F., Hardy, J., Quinn, N., et al. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.172 · Cited by 153 · see citing works
Goldman, J. G., Stebbins, G. T., Dinh, V., Bernard, B. A., Merkitch, D., deToledo‐Morrell, L., & Goetz, C. G. (2014) · Brain · doi:10.1093/brain/awt360 · Cited by 152 · see citing works
Self-citationRegional patterns of brain tissue loss associated with depression in Parkinson disease
Kostić, V., Agosta, F., Petrović, I., Galantucci, S., Špica, V., Ječmenica-Lukić, M., & Filippi, M. (2010) · Neurology · doi:10.1212/wnl.0b013e3181f11c1d · Cited by 149 · see citing works
Clinical implications of delayed orthostatic hypotension
Gibbons, C. H., & Freeman, R. L. (2015) · Neurology · doi:10.1212/wnl.0000000000002030 · Cited by 148 · see citing works
Lang, A. E. (2011) · Movement Disorders · doi:10.1002/mds.23609 · Cited by 146 · cited 1× · see citing works
“These motor signs are often preceded by nonmotor manifestations such as olfactory dysfunction in approximately 90%, constipation, REM behavior disorder, and depression/anxiety.(24) As the disease progresses, the clinical picture becomes a composite of levodopa-related motor complications, nondopaminergic motor feature…”
Self-citationNew methods for the assessment of Parkinson's disease (2005 to 2015): A systematic review
Sánchez‐Ferro, Á., Elshehabi, M., Godinho, C., Salkovic, D., Hobert, M. A., Domingos, J., van Uem, J. M., Ferreira, J. J., & Maetzler, W. (2016) · Movement Disorders · doi:10.1002/mds.26723 · Cited by 145 · cited 1× · see citing works
“applications to noninvasively monitor mobility and motor speed on a large scale.(225) 2.”
Intracranial Self-Stimulation in Man
Bishop, M. P., Elder, S. T., & Heath, R. G. (1963) · Science · doi:10.1126/science.140.3565.394 · Cited by 142 · cited 1× · see citing works
“DBS had been used since the 1960s for a number of psychiatric and pain disorders.(188) It had been used sporadically to treat movement disorders in the 1970s and 1980s, but it was the introduction of STN DBS by Benabid and Pollak and their team that caused a major impact, only comparable to the one seen when levodopa…”
Marras, C., Lang, A., van de Warrenburg, B. V. D., Sue, C., Tabrizi, S., Bertram, L., Mercimek-Mahmutoglu, S., Ebrahimi-Fakhari, D., Warner, T., Durr, A., et al. (2017) · Movement Disorders · doi:10.1002/mds.27045 · Cited by 141 · see citing works
Self-citationParkinson's disease patients show reduced cortical‐subcortical sensorimotor connectivity
Sharman, M. A., Valabrègue, R., Perlbarg, V., Marrakchi‐Kacem, L., Vidailhet, M., Benali, H., Brice, A., & Lehéricy, S. (2012) · Movement Disorders · doi:10.1002/mds.25255 · Cited by 140 · cited 1× · see citing works
“Reduced connectivity of the SN with the basal ganglia and thalamus were also evidenced in PD patients using tractography-based methods and resting state functional connectivity.(91) In contrast to quantitative mapping, measurements of the morphological changes of the SN seemed unreliable to detect changes related to P…”
Chemopallidectomy and Chemothalamectomy
Cooper, I. S., & Bravo, G. (1958) · Journal of neurosurgery · doi:10.3171/jns.1958.15.3.0244 · Cited by 139 · see citing works
Muthuraman, M., Heute, U., Arning, K., Anwar, A. R., Elble, R., Deuschl, G., & Raethjen, J. (2012) · NeuroImage · doi:10.1016/j.neuroimage.2012.01.088 · Cited by 134 · see citing works
Self-citationM itochondrial DNA and primary mitochondrial dysfunction in P arkinson's disease
Giannoccaro, M. P., Morgia, C. L., Rizzo, G., & Carelli, V. (2017) · Movement Disorders · doi:10.1002/mds.26966 · Cited by 134 · cited 1× · see citing works
“function either by regulating oxidant defenses, mitophagy, or biogenesis.(250) Together, these observations T H E S H A K I N G P A L S Y : P A S T , P R E S E N T A N D F U T U R E”
Correlation of striatal dopamine transporter imaging with post mortem substantia nigra cell counts
Kraemmer, J., Kovacs, G. G., Perju-Dumbrava, L., Pirker, S., Traub-Weidinger, T., & Pirker, W. (2014) · Movement Disorders · doi:10.1002/mds.25975 · Cited by 132
Neuropathology of α‐synuclein propagation and braak hypothesis
McCann, H., Cartwright, H., & Halliday, G. M. (2015) · Movement Disorders · doi:10.1002/mds.26421 · Cited by 132 · cited 2× · see citing works
“The time course of pathological progression is usually very slow, with 50% of patients having limbic LPs on average 13 years following onset, and all having such pathology by 18 years.(75) In patients with Alzheimer pathology (often older at onset), LPs dominate the limbic system and only later may become more widespr…”
Self-citationTrophic Factor Gene Therapy for Parkinson's Disease
Kordower, J. H., & Björklund, A. (2013) · Movement Disorders · doi:10.1002/mds.25344 · Cited by 129 · cited 3× · see citing works
“Of these, none have received as much attention as members of the glial family of ligands, glial derived neurotrophic factor (GDNF) and neurturin.(275) GDNF was first shown to support the viability of midbrain dopaminergic neurons in culture.”
InfluentialSelf-citationDefining at‐risk populations for Parkinson's disease: Lessons from ongoing studies
Berg, D., MAREK, K. L., Ross, G. W., & Poewe, W. H. (2012) · Movement Disorders · doi:10.1002/mds.24985 · Cited by 128 · cited 1× · see citing works
“In a population-based study, increased echogenic signal was associated with a 20-fold increased risk of PD (although RBD studies have been more uncertain).(223) Hyperechogenicity is present early in PD and in general more pronounced contralaterally to the clinically more affected side.”
Self-citationCurrent applications and limitations of surgical treatments for movement disorders
Krack, P., Martinez‐Fernandez, R., del Alamo, M., & Obeso, J. A. (2017) · Movement Disorders · doi:10.1002/mds.26890 · Cited by 122 · cited 1× · see citing works
“ICD behaviors typically resolve after discontinuing DA treatment; however, some patients develop a DA withdrawal syndrome.(61) The relationship between DBS and ICDs is complex, with both improvement and worsening reported post-DBS surgery.”
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27 of the 308 references couldn’t be matched to a known paper.
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Parkinson’s disease: etiopathogenesis and treatment
Jankovic, J. J., & Tan, E. K. (2020) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2019-322338 · Cited by 1,185 · see citing works
Self-citationSmajić, S., Prada-Medina, C. A., Landoulsi, Z., Ghelfi, J., Delcambre, S., Dietrich, C., Jarazo, J., Henck, J., Balachandran, S., Pachchek, S., et al. (2022) · Brain · doi:10.1093/brain/awab446 · Cited by 590 · see citing works
“Approximately 95% of Parkinson’s disease patients do not harbour an interpretable genetic cause; therefore, they are classified as idiopathic Parkinson’s disease.(4)”
The genetics of Parkinson disease
Deng, H., Wang, P., & Jankovic, J. (2018) · Ageing Research Reviews · doi:10.1016/j.arr.2017.12.007 · Cited by 530 · see citing works
Self-citationParkinson disease and the immune system - Associations, mechanisms and therapeutics
Tan, E.-K., Chao, Y.-X., West, A., Chan, L.-L., Poewe, W., & Jankovic, J. (2020) · Nature Reviews Neurology · doi:10.1038/s41582-020-0344-4 · Cited by 457 · see citing works
Self-citationGe, P., Dawson, V. L., & Dawson, T. M. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00367-7 · Cited by 514 · see citing works
Metagenomics of Parkinson’s disease implicates the gut microbiome in multiple disease mechanisms
Wallen, Z. D., Demirkan, A., Twa, G., Cohen, G., Dean, M. N., Standaert, D. G., Sampson, T. R., & Payami, H. (2022) · Nature Communications · doi:10.1038/s41467-022-34667-x · Cited by 346 · see citing works
Self-citationLang, A. E., & Espay, A. J. (2018) · Movement Disorders · doi:10.1002/mds.27360 · Cited by 374 · see citing works
Self-citationNeuropathology and molecular diagnosis of Synucleinopathies
Koga, S., Sekiya, H., Kondru, N. C., Ross, O. A., & Dickson, D. W. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00501-z · Cited by 345 · see citing works
Targeting Alpha-Synuclein as a Therapy for Parkinson’s Disease
Fields, C. R., Bengoa‐Vergniory, N., & Wade‐Martins, R. (2019) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2019.00299 · Cited by 336 · see citing works
“PD is characterized by motor symptoms including tremor, rigidity, bradykinesia, postural instability, gait and balance impairment and non-motor symptoms such as cognitive decline, autonomic impairment, rapid eye movement behavioral sleep disorder, constipation, and other behavioral disturbances (Stacy, 2011; Obeso et…”
BackgroundThe role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options
Wang, Q., Luo, Y., Ray Chaudhuri, K., Reynolds, R., Tan, E.-K., & Pettersson, S. (2021) · Brain · doi:10.1093/brain/awab156 · Cited by 281 · see citing works
Liu, Y., Ma, X., Fujioka, H., Liu, J., Chen, S., & Zhu, X. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1906565116 · Cited by 299 · see citing works
Therapeutic strategies for Parkinson disease: beyond dopaminergic drugs
Charvin, D., Medori, R., Hauser, R. A., & Rascol, O. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2018.136 · Cited by 285 · see citing works
Hou, Y.-F., Shan, C., Zhuang, S.-Y., Zhuang, Q.-Q., Ghosh, A., Zhu, K.-C., Kong, X.-K., Wang, S.-M., Gong, Y.-L., Yang, Y.-Y., et al. (2021) · Microbiome · doi:10.1186/s40168-020-00988-6 · Cited by 231 · see citing works
Mitochondria and Parkinson’s Disease: Clinical, Molecular, and Translational Aspects
Borsche, M., Pereira, S. L., Klein, C., & Grünewald, A. (2020) · Journal of Parkinson s Disease · doi:10.3233/jpd-201981 · Cited by 276 · see citing works
“Despite significant advances in deciphering the pathophysiology of PD [2], the etiology remains elusive for the majority of cases.”
BackgroundSelf-citationEvolving concepts on bradykinesia.
Bologna, M., Paparella, G., Fasano, A., Hallett, M., & Berardelli, A. (2019) · Brain : a journal of neurology · doi:10.1093/brain/awz344 · Cited by 233 · see citing works
Self-citationMarsili, L., Rizzo, G., & Colosimo, C. (2018) · Frontiers in Neurology · doi:10.3389/fneur.2018.00156 · Cited by 244 · see citing works
“In the early 19th century, James Parkinson published his essay on “The Shaking Palsy,” in which he described in detail the clinical features (tremor, flexed posture, and festination) of a new disease with an insidious onset and a progressive disabling course called paralysis agitans; he was inspired by the observation…”
BackgroundMethodInfluentialProdromal Parkinson's Disease: The Decade Past, the Decade to Come
Postuma, R. B., & Berg, D. (2019) · Movement Disorders · doi:10.1002/mds.27670 · Cited by 224 · see citing works
“However, LRRK-2 and GBA mutations are relatively common in PD, with sufficiently high penetrance to warrant collection.(64) These mutation carriers are also an important potential group in which to test neuroprotective interventions (targeted therapy like LRRK-2 inhibitors, enzyme replacement or substrate-reduction th…”
BackgroundSelf-citationBido, S., Muggeo, S., Massimino, L., Marzi, M. J., Giannelli, S. G., Melacini, E., Nannoni, M., Gambarè, D., Bellini, E., Ordazzo, G., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-26519-x · Cited by 190 · see citing works
Rahman, M. H., Bajgai, J., Fadriquela, A., Sharma, S., Trinh, T. T., Akter, R., Jeong, Y. J., Goh, S. H., Kim, C.-S., & Lee, K.-J. (2021) · Molecules · doi:10.3390/molecules26175327 · Cited by 182 · see citing works
“To summarize, natural products have recently received increasing interest as alternative or integrative treatment agents against AD and other NDs [18,19].”
BackgroundZesiewicz, T. (2019) · CONTINUUM Lifelong Learning in Neurology · doi:10.1212/con.0000000000000764 · Cited by 86 · see citing works
<i>APOE</i> genotype regulates pathology and disease progression in synucleinopathy
Davis, A. A., Inman, C. E., Wargel, Z. M., Dube, U., Freeberg, B. M., Galluppi, A., Haines, J. N., Dhavale, D. D., Miller, R., Choudhury, F. A., et al. (2020) · Science Translational Medicine · doi:10.1126/scitranslmed.aay3069 · Cited by 177 · see citing works
Marchetti, B., Tirolo, C., L’Episcopo, F., Caniglia, S., Testa, N., Smith, J. A., Pluchino, S., & Serapide, M. F. (2020) · Aging Cell · doi:10.1111/acel.13101 · Cited by 185 · see citing works
“…there are no effective treatments that can stop or reverse the neurodegeneration process in PD and current treatments rely on DAergic drugs, including levodopa (L-DOPA) and DAergic agonists, which only temporarily alleviate motor symptoms (Obeso et al., 2017; Olanow, 2019; Olanow & Schapira, 2013).”
BackgroundInfluentialRotenone-Induced Model of Parkinson’s Disease: Beyond Mitochondrial Complex I Inhibition
Ibarra-Gutiérrez, M. T., Serrano‐García, N., & Orozco‐Ibarra, M. (2023) · Molecular Neurobiology · doi:10.1007/s12035-022-03193-8 · Cited by 173 · see citing works
“Their primary function is to receive, integrate, and process the information that comes from the cortex, sending it to the thalamus, which stimulates or inhibits the activity of the frontal motor areas of the cerebral cortex, which are responsible for regulating motor activity, through the called direct and indirect p…”
BackgroundInfluentialPostural Instability in Parkinson’s Disease: A Review
Palakurthi, B., & Burugupally, S. P. (2019) · Brain Sciences · doi:10.3390/brainsci9090239 · Cited by 165 · see citing works
“Environmental factors such as living in rural areas, pesticide exposure, coffee consumption, smoking cigarettes, and drinking alcohol are believed to have a role in causing PD [3,67].”
BackgroundDiet in Parkinson’s Disease: Critical Role for the Microbiome
Jackson, A., Forsyth, C. B., Shaikh, M., Voigt, R. M., Engen, P. A., Ramirez, V., & Keshavarzian, A. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2019.01245 · Cited by 145 · see citing works
The Neuropsychiatry of Parkinson Disease: A Perfect Storm
Weintraub, D. A., & Mamikonyan, E. (2019) · American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2019.03.002 · Cited by 164 · see citing works
Self-citationMehanna, R., Śmiłowska, K., Fleisher, J. E., Post, B., Hatano, T., Piemonte, M. E. P., Kumar, K. R., McConvey, V., Zhang, B., Tan, E., et al. (2022) · Movement Disorders Clinical Practice · doi:10.1002/mdc3.13523 · Cited by 155 · see citing works
A Cortical Pathogenic Theory of Parkinson’s Disease
Foffani, G., & Obeso, J. A. (2018) · Neuron · doi:10.1016/j.neuron.2018.07.028 · Cited by 161 · see citing works
Self-citationEnergy Metabolism Decline in the Aging Brain—Pathogenesis of Neurodegenerative Disorders
Błaszczyk, J. W. (2020) · Metabolites · doi:10.3390/metabo10110450 · Cited by 162 · see citing works
“Neurogenesis, and the subsequent formation or modification of functional networks in the aging brain, are substantially impaired, due to progressing energy deficit and damages to the glymphatic system [137].”
BackgroundArcusa, R., Villaño, D., Marhuenda, J., Cano, M., Cerdá, B., & Zafrilla, P. (2022) · Frontiers in Nutrition · doi:10.3389/fnut.2022.809621 · Cited by 176 · see citing works
Young-onset Parkinson's disease: Its unique features and their impact on quality of life
Mehanna, R., & Jankovic, J. J. (2019) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2019.06.001 · Cited by 142 · see citing works
Self-citationRabie, H., Zhang, Y., Pasquale, N. J., Lagos, M. J., Batson, P. E., & Lee, K. (2019) · Advanced Materials · doi:10.1002/adma.201806991 · Cited by 155 · see citing works
Functional neuroanatomy of the basal ganglia
Jankovic, J. J., Hallett, M., Okun, M. S., Comella, C., Fahn, S., & Goldman, J. G. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-31071-0.00003-2 · Cited by 4 · see citing works
Self-citationAnimal Models for Parkinson’s Disease Research: Trends in the 2000s
Kin, K., Yasuhara, T., Kameda, M., & Date, I. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20215402 · Cited by 137 · see citing works
“Although these treatments reduce motor symptoms and improve the patient’s quality of life [7], clinical needs for new therapies to prevent, stop, or slow disease progression are not fully understood.”
BackgroundQuadri, M., Mandemakers, W., Grochowska, M. M., Masius, R., Geut, H., Fabrizio, E., Breedveld, G. J., Kuipers, D., Minneboo, M., Vergouw, L. J. M., et al. (2018) · The Lancet Neurology · doi:10.1016/s1474-4422(18)30179-0 · Cited by 143 · see citing works
The pathophysiology of Parkinson's disease tremor
Dirkx, M. F., & Bologna, M. (2022) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2022.120196 · Cited by 131 · see citing works
“This raises the possibility that dopamine-resistance of tremor is a dose dependent phenomenon [25], suggesting that tremor sometimes requires higher doses of dopamine than the other motor symptoms.”
BackgroundThe human olfactory system in two proteinopathies: Alzheimer’s and Parkinson’s diseases
Úbeda‐Bañón, I., Saiz‐Sánchez, D., Flores‐Cuadrado, A., Corroto, E. R., González-Rodríguez, M., Villar‐Conde, S., Astillero‐Lopez, V., Cabello, J. P., Gallardo‐Alcañiz, M. J., Vaamonde‐Gamo, J., et al. (2020) · Translational Neurodegeneration · doi:10.1186/s40035-020-00200-7 · Cited by 129 · see citing works
“Neuropathologically, Parkinson’s disease includes neuronal loss in the ventrolateral tier of the substantia nigra pars compacta and the corresponding striatal dopamine denervation and widespread intracellular α-synuclein accumulation [2, 53, 54].”
BackgroundRuppert, M. C., Greuel, A., Tahmasian, M., Schwartz, F., Stürmer, S., Maier, F., Hammes, J., Tittgemeyer, M., Timmermann, L., van Eimeren, T., et al. (2020) · Brain · doi:10.1093/brain/awaa019 · Cited by 119 · see citing works
Clinical and Imaging Markers of Prodromal Parkinson's Disease
Hustad, E., & Aasly, J. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.00395 · Cited by 105 · see citing works
Parkinson’s disease: experimental models and reality
Jiang, P., & Dickson, D. W. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1788-5 · Cited by 113 · see citing works
“Although it has been two centuries since the description of shaking palsy by James Parkinson [144], the etiology of this disease remains enigmatic.”
Clinical Diagnostic Accuracy of Parkinson's Disease: Where Do We Stand?
Virameteekul, S., Révész, T., Jaunmuktane, Z., Warner, T. T., & Pablo‐Fernández, E. D. (2023) · Movement Disorders · doi:10.1002/mds.29317 · Cited by 111 · see citing works
Neuronal vulnerability in Parkinson disease: Should the focus be on axons and synaptic terminals?
Wong, Y. C., Luk, K. C., Purtell, K., Burke, S., Stoessl, A. J., Trudeau, L., Yue, Z., Krainc, D., Oertel, W. H., Obeso, J. A., et al. (2019) · Movement Disorders · doi:10.1002/mds.27823 · Cited by 123 · see citing works
“The second half of the 20th century produced remarkable advances in defining neurodegeneration of the nigrostriatal dopaminergic projection as the primary basis for PD and major therapeutic developments such as levodopa and DBS.1 Thus, clinical management of PD has improved substantially, diagnosis of genetic forms is…”
BackgroundSelf-citationConcordance for Parkinson's disease in twins: A 20‐year update
Goldman, S. M., MAREK, K. L., Ottman, R., Meng, C., Comyns, K., Chan, P., Ma, J., Marras, C., Langston, J. W., Ross, G. W., et al. (2019) · Annals of Neurology · doi:10.1002/ana.25441 · Cited by 114 · see citing works
“Despite identification of multiple genes associated with Parkinson’s disease (PD) risk, the cause of most PD remains unknown.(1) During the 1990s, we conducted a cross-sectional study of PD in 19,842 members of the National Academy of Sciences Twin Registry (Twin Registry), a cohort established during the 1960s of whi…”
BackgroundSelf-citationCerebral differences between dopamine-resistant and dopamine-responsive Parkinson’s tremor
Dirkx, M. F., Zach, H., van Nuland, A. J. M., Bloem, B. R., Toni, I., & Helmich, R. C. G. (2019) · Brain · doi:10.1093/brain/awz261 · Cited by 102 · see citing works
“This would fit the theory that tremor suppression is a threshold phenomenon with respect to the dose of levodopa required (Obeso et al., 2017).”
BackgroundSzego, E. M., Malz, L., Bernhardt, N., Rösen-Wolff, A., Falkenburger, B. H., & Luksch, H. (2022) · eLife · doi:10.7554/elife.81943 · Cited by 94 · see citing works
The Pathology of Parkinson’s Disease and Potential Benefit of Dietary Polyphenols
Aryal, S., Skinner, T., Bridges, B., & Weber, J. T. (2020) · Molecules · doi:10.3390/molecules25194382 · Cited by 109 · see citing works
Innate and adaptive immune responses in Parkinson's disease
Schonhoff, A. M., Williams, G. P., Wallen, Z. D., Standaert, D. G., & Harms, A. S. (2019) · Progress in brain research · doi:10.1016/bs.pbr.2019.10.006 · Cited by 115 · see citing works
Self-citationPeripheral Immune Profile and Neutrophil‐to‐Lymphocyte Ratio in Parkinson's Disease
Muñoz-Delgado, L., Macías-García, D., Jesús, S., Martín-Rodríguez, J. F., Labrador-Espinosa, M., Jiménez-Jaraba, M. D. V., Adarmes-Gómez, A., Carrillo, F., & Mir, P. (2021) · Movement Disorders · doi:10.1002/mds.28685 · Cited by 89 · see citing works
“Parkinson’s disease (PD) is one of the most common neurodegenerative disorders.(1) The etiopathogenesis of PD remains unclear, but current evidence points to neuroinflammation as a major contributor to the etiology and progression of neurodegeneration in PD.”
BackgroundIn vivo functional diversity of midbrain dopamine neurons within identified axonal projections
Farassat, N., Costa, K. M., Stojanovic, S., Albert, S., Kovacheva, L., Shin, J., Egger, R., Somayaji, M., Duvarci, S., Schneider, G., et al. (2019) · eLife · doi:10.7554/elife.48408 · Cited by 94 · see citing works
The gut microbiome in Parkinson's disease: A culprit or a bystander?
Keshavarzian, A., Engen, P. A., Bonvegna, S., & Cilia, R. (2020) · Progress in brain research · doi:10.1016/bs.pbr.2020.01.004 · Cited by 104 · see citing works
Gene therapy reduces Parkinson’s disease symptoms by reorganizing functional brain connectivity
Niethammer, M., Tang, C. C., Vo, A., Nguyen, N., Spetsieris, P. G., DHAWAN, V. M., Ma, Y., SMALL, M. P., Feigin, A., During, M. J., et al. (2018) · Science Translational Medicine · doi:10.1126/scitranslmed.aau0713 · Cited by 99 · see citing works
The heterogeneity of Parkinson’s disease
Wüllner, U., Borghammer, P., Choe, C., Csóti, I., Falkenburger, B. H., Gasser, T., Lingor, P., & Riederer, P. F. (2023) · Journal of Neural Transmission · doi:10.1007/s00702-023-02635-4 · Cited by 132 · see citing works
Progressive parkinsonism in older adults is related to the burden of mixed brain pathologies
Buchman, A. S., Yu, L., Wilson, R. S., Leurgans, S. E., Nag, S., Shulman, J. M., Barnes, L. L., Schneider, J. A., & Bennett, D. A. (2019) · Neurology · doi:10.1212/wnl.0000000000007315 · Cited by 125 · see citing works
“Hence, identifying clinical antecedents of PD prior to its clinical diagnosis, prodromal PD, offers the potential for early intervention and prevention.(5) While PD is uncommon, accumulating evidence suggests that parkinsonism, a heterogeneous disorder, may affect more than half of older adults by age 85.”
BackgroundL’Episcopo, F., Tirolo, C., Serapide, M. F., Caniglia, S., Testa, N., Leggio, L., Vivarelli, S., Iraci, N., Pluchino, S., & Marchetti, B. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00012 · Cited by 84 · see citing works
“…on dopamine replacement therapy, using the metabolic precursor of dopamine, L-DOPA, or dopamine receptor agonists, albeit they only temporally alleviate the motor symptoms without stopping the ongoing neurodegeneration (Olanow and Schapira, 2013; Obeso et al., 2017, for a comprehensive review).”
MethodHelley, M., Pinnell, J. R., Sportelli, C., & Tieu, K. (2017) · Frontiers in Genetics · doi:10.3389/fgene.2017.00177 · Cited by 95 · see citing works
“It has been proposed that this process involves a combination of selective expression of L-type Ca2+ channel leading to elevated cytosolic Ca2+, oxidized cytosolic dopamine, α-synuclein and the inherent long, highly branched axons of nigral dopaminergic neurons (Obeso et al., 2017).”
BackgroundCalcium, Bioenergetics, and Parkinson’s Disease
Zampese, E., & Surmeier, D. J. (2020) · Cells · doi:10.3390/cells9092045 · Cited by 79 · see citing works
“These neurons—whose degeneration is responsible for the core motor symptoms of Parkinson’s disease (PD) [6,7]—have large cytosolic oscillations in Ca2+ concentration ([Ca2+]).”
BackgroundSelf-citationCav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease
Benkert, J., Heß, S., Roy, S., Beccano-Kelly, D. A., Burkert, N., Duda, J., Simons, C., Patil, K., Gaifullina, A., Mannal, N., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-12834-x · Cited by 95 · see citing works
Parkinson disease and the risk of epileptic seizures
Gruntz, K., Bloechliger, M., Becker, C., Jick, S. S., Fuhr, P., Meier, C. R., & Rüegg, S. J. (2018) · Annals of Neurology · doi:10.1002/ana.25157 · Cited by 97 · see citing works
Chatterjee, D., Bhatt, M. A., Butler, D., Genst, E. D., Dobson, C. M., Messer, A. C., & Kordower, J. H. (2018) · npj Parkinson s Disease · doi:10.1038/s41531-018-0062-4 · Cited by 93 · see citing works
Self-citationSavitt, D., & Jankovic, J. J. (2019) · Drugs · doi:10.1007/s40265-019-01104-1 · Cited by 89 · see citing works
“The accumulation of misfolded α-syn into pathological aggregates is believed to play a central role in the pathogenesis of PD [2].”
BackgroundSelf-citationDevelopment of early diagnosis of Parkinson's disease: Illusion or reality?
Ugrumov, M. V. (2020) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.13429 · Cited by 90 · see citing works
Deep brain stimulation-guided optogenetic rescue of parkinsonian symptoms
Valverde, S., Vandecasteele, M., Piette, C., Derousseaux, W., Gangarossa, G., Aristieta, A., Touboul, J. D., Degos, B., & Venance, L. (2020) · Nature Communications · doi:10.1038/s41467-020-16046-6 · Cited by 88 · see citing works
Basal lamina changes in neurodegenerative disorders
Nguyen, B., Bix, G., & Yao, Y. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00502-y · Cited by 75 · see citing works
“Typical symptoms of PD include resting tremor, gait disorders, and bradykinesia [303].”
BackgroundCell models for Alzheimer’s and Parkinson’s disease: At the interface of biology and drug discovery
Cetin, S., Knez, D., Gobec, S., Kos, J., & Pišlar, A. H. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.112924 · Cited by 87 · see citing works
Diabetes, a Contemporary Risk for Parkinson’s Disease: Epidemiological and Cellular Evidences
Sergi, D., Renaud, J., Simola, N., & Martinoli, M. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00302 · Cited by 85 · see citing works
“Disease-causing duplications (Chartier-Harlin et al., 2004) and triplications (Singleton et al., 2003) of the SNCA gene were identified, and other genes were added in subsequent years (Obeso et al., 2017).”
BackgroundMadrid, J., & Benninger, D. H. (2020) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2020.108957 · Cited by 87 · see citing works
Amin, R., Quispe, C., Docea, A. O., Ydyrys, A., Kulbayeva, M., Durna Daştan, S., Calina, D., & Sharifi-Rad, J. (2022) · Neurochemistry International · doi:10.1016/j.neuint.2022.105376 · Cited by 74 · see citing works
Alpha-Synuclein as a Prominent Actor in the Inflammatory Synaptopathy of Parkinson’s Disease
Cardinale, A., Calabrese, V., de Iure, A., & Picconi, B. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126517 · Cited by 79 · see citing works
“The reduction of striatal dopaminergic neurons triggers motor symptoms that include bradykinesia, uncontrollable tremor at rest, postural impairment, and rigidity, which together characterise Parkinson’s disease (PD) as a movement disorder [1,2].”
BackgroundLin, K.-L., Lin, K.-J., Wang, P., Chuang, J., Lin, H., Chen, S., Chuang, Y., Huang, S., Tiao, M., Chen, J., et al. (2018) · Free Radical Research · doi:10.1080/10715762.2018.1489128 · Cited by 78 · see citing works
“Although highly efficacious pharmacological therapies have become available, none of these are curative and PD remains a progressive disorder [3,4].”
BackgroundThe Misfolding Mystery: α-syn and the Pathogenesis of Parkinson's Disease.
Negi, S., Khurana, N., & Duggal, N. (2024) · Neurochemistry International · doi:10.1016/j.neuint.2024.105760 · Cited by 68 · see citing works
Sproviero, D., Gagliardi, S., Zucca, S., Arigoni, M., Giannini, M., Garofalo, M., Olivero, M., Dell’Orco, M., Pansarasa, O., Bernuzzi, S., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22052737 · Cited by 75 · see citing works
“In PD degeneration of dopaminergic pigmented neurons in the substantia nigra (SN) and accumulation of α-synuclein protein, which is the main component of Lewy bodies (LBs), are the main features [5].”
BackgroundAnimal Models of Metabolic Disorders in the Study of Neurodegenerative Diseases: An Overview
Bem, A. F. D., Krolow, R., Farias, H. R., de Rezende, V. L., Gelain, D. P., Moreira, J. C. F., Duarte, J. M. N., & de Oliveira, J. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.604150 · Cited by 64 · see citing works
“Parkinson’s disease is the second most prevalent neurodegenerative disease after AD, and the most common movement disorder (Obeso et al., 2017).”
BackgroundThe role of T cells in the pathogenesis of Parkinson’s disease
Chen, Z., Chen, S., & Liu, J. (2018) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.08.002 · Cited by 78 · see citing works
Zhang, J., Culp, M. L., Craver, J., & Darley-Usmar, V. M. (2018) · Journal of Neurochemistry · doi:10.1111/jnc.14308 · Cited by 73 · see citing works
Insights into Parkinson’s disease from computational models of the basal ganglia
Humphries, M. D., Obeso, J. A., & Dreyer, J. K. (2018) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2017-315922 · Cited by 73 · see citing works
Self-citationTranscranial Temporal Interference Stimulation of the Right Globus Pallidus in Parkinson's Disease
Yang, C., Xu, Y.-X., Feng, X.-F., Wang, B., Du, Y., Wang, K., Lu, J.-J., Huang, L.-Y., Qian, Z., Wang, Z., et al. (2024) · Movement Disorders · doi:10.1002/mds.29967 · Cited by 65 · see citing works
Neuroprotective Mechanisms of Ginsenoside Rb1 in Central Nervous System Diseases
Gong, L., Yin, J., Zhang, Y., Ren, H., Lou, Y., Jiang, H., Sun, L., Jia, J., & Zeng, X. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.914352 · Cited by 68 · see citing works
“Parkinson Disease (PD), one of the most common neurodegenerative diseases (Obeso et al., 2017), is characterized by the loss of dopaminergic neurons in the substantia nigra of midbrain (Zeng et al., 2014a).”
BackgroundCLR01 protects dopaminergic neurons in vitro and in mouse models of Parkinson’s disease
Bengoa-Vergniory, N., Faggiani, E., Ramos-Gonzalez, P., Kirkiz, E., Connor-Robson, N., Brown, L. V., Siddique, I., Li, Z., Vingill, S., Cioroch, M., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-18689-x · Cited by 64 · see citing works
Clinical severity in Parkinson’s disease is determined by decline in cortical compensation
Johansson, M. E., Toni, I., Kessels, R. P. C., Bloem, B. R., & Helmich, R. C. G. (2023) · Brain · doi:10.1093/brain/awad325 · Cited by 63 · see citing works
“4,5 6-11 It remains unclear to what extent such compensatory processes, along with interindividual differences in their efficacy, contribute to clinical heterogeneity in Parkinson’s disease, over and above basal ganglia dysfunction.”
Neuroinflammation in Parkinson’s Disease: Triggers, Mechanisms, and Immunotherapies
Wang, T., Shi, C., Luo, H., Zheng, H., Fan, L., Tang, M., Su, Y., Yang, J., Mao, C., & Xu, Y. (2021) · The Neuroscientist · doi:10.1177/1073858421991066 · Cited by 66 · see citing works
Advances in Proteomic and Metabolomic Profiling of Neurodegenerative Diseases
Schuh, A. F. S., Bieger, A., Borelli, W. V., Portley, M. K., Awad, P. S., & Bandrés‐Ciga, S. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2021.792227 · Cited by 63 · see citing works
Nguyen, A. P. T., Tsika, E., Kelly, K., Levine, N. D., Chen, X., West, A. B., Boularand, S., Barnéoud, P., & Moore, D. J. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1922184117 · Cited by 70 · see citing works
“P disease (PD) typically occurs in a sporadic manner through a complex interaction between genetic risk, aging, and environmental exposure (1).”
A Review on Wearable Technologies for Tremor Suppression
Lora-Millan, J. S., Delgado-Oleas, G., Benito-León, J., & Rocon, E. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.700600 · Cited by 62 · see citing works
Lipidomics of Bioactive Lipids in Alzheimer’s and Parkinson’s Diseases: Where Are We?
Chiurchiù, V., Tiberi, M., Matteocci, A., Fazio, F., Siffeti, H., Saracini, S., Mercuri, N. B., & Sancesario, G. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116235 · Cited by 65 · see citing works
“One of the neuropathophysiological hallmarks of PD is characterized by the accumulation of α-synuclein (α-syn) and the formation of filamentous aggregates called “Lewy bodies” in the brainstem, limbic system, and cortical areas, leading to a progressive loss of dopaminergic neurons in the substantia nigra and striatum…”
BackgroundEspinoza, S., Scarpato, M., Damiani, D., Managò, F., Mereu, M., Contestabile, A., Peruzzo, O., Carninci, P., Santoro, C., Papaleo, F., et al. (2019) · Molecular Therapy · doi:10.1016/j.ymthe.2019.08.005 · Cited by 66 · see citing works
“Although familial PD (about 5% of the total cases) has been important to unveil the molecular pathways involved in neurodegeneration, most of the PD patients are sporadic.(2) Currently, no treatments are available that can slow or arrest neurodegeneration.”
BackgroundAn update on immune-based alpha-synuclein trials in Parkinson’s disease
Alfaidi, M., Barker, R. A., & Kuan, W. (2024) · Journal of Neurology · doi:10.1007/s00415-024-12770-x · Cited by 71 · see citing works
Lee, S.-B., Kim, Y.-J., Hwang, S., Son, H., Lee, S.-K., Park, K.-I., & Kim, Y.-G. (2022) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2022.01.011 · Cited by 60 · see citing works
Parkinson’s Disease-Related Genes and Lipid Alteration
Fais, M., Dore, A., Galioto, M., Galleri, G., Crosio, C., & Iaccarino, C. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22147630 · Cited by 68 · see citing works
“The etiology of PD is unknown, although older age and neurotoxins are established risk factors, and smoking appears to be protective [1].”
Backgroundα-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment
Karim, M. R., Liao, E. E., Kim, J., Meints, J. P., Martínez, H., Pletniková, O., Troncoso, J. C., & Lee, M. K. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00364-w · Cited by 66 · see citing works
Immunotherapy in Parkinson’s disease: Current status and future directions
Chatterjee, D., & Kordower, J. H. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104587 · Cited by 68 · see citing works
Self-citationAgerschou, E. D., Saridaki, T., Flagmeier, P., Galvagnion, C., Komnig, D., Nagpal, A., Gasterich, N., Heid, L. F., Prasad, V., Shaykhalishahi, H., et al. (2019) · eLife · doi:10.7554/elife.46112 · Cited by 71 · see citing works
Peripheral Inflammation Is Associated with Dopaminergic Degeneration in Parkinson's Disease
Muñoz‐Delgado, L., Labrador‐Espinosa, M. Á., Macías‐García, D., Jesús, S., Zamora, B. B., Fernández‐Rodríguez, P., Adarmes-Gómez, A. D., Castillo, M. I. R., Castro‐Labrador, S., Silva‐Rodríguez, J., et al. (2023) · Movement Disorders · doi:10.1002/mds.29369 · Cited by 61 · see citing works
“Following the neurodegeneration of the SNpc, a depletion of dopamine is observed through the nigrostriatal pathways, which is mainly responsible for the cardinal motor symptoms of PD.(2,3) The dopaminergic neurodegeneration associated with PD can be assessed in vivo by using [(123)I]FP-CIT single photon emission compu…”
BackgroundMethodResultInfluentialHill, B. G., Shiva, S., Ballinger, S. W., Zhang, J., & Darley-Usmar, V. M. (2019) · Biological Chemistry · doi:10.1515/hsz-2019-0268 · Cited by 65 · see citing works
Role of Microgliosis and NLRP3 Inflammasome in Parkinson’s Disease Pathogenesis and Therapy
de Araújo, F. M., Cuenca‐Bermejo, L., Fernández‐Villalba, E., Costa, S. L., da Silva, V. D. A., & Herrero, M. T. (2021) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-020-01027-6 · Cited by 61 · see citing works
Otomo, K., Perkins, J., Kulkarni, A. S., Stojanovic, S., Roeper, J., & Paladini, C. A. (2020) · Nature Communications · doi:10.1038/s41467-020-20041-2 · Cited by 53 · see citing works
Extracellular Vesicles as Novel Diagnostic and Prognostic Biomarkers for Parkinson’s Disease
Leggio, L., Paternò, G., Vivarelli, S., Falzone, G. G., Giachino, C., Marchetti, B., & Iraci, N. (2021) · Aging and disease · doi:10.14336/ad.2021.0527 · Cited by 55 · see citing works
“Of note, while providing a symptomatic relief [15, 23], these drugs do not modify the progressive neurodegenerative cell loss associated with PD, and in many cases, they result in debilitating side-effects [15].”
BackgroundPeripheral inflammatory immune response differs among sporadic and familial Parkinson’s disease
Muñoz‐Delgado, L., Macías‐García, D., Periñán, M. T., Jesús, S., Adarmes-Gómez, A. D., Bonilla‐Toribio, M., Buiza‐Rueda, D., Jiménez‐Jaraba, M. V., Zamora, B. B., Belloso, R. D., et al. (2023) · npj Parkinson s Disease · doi:10.1038/s41531-023-00457-5 · Cited by 62 · see citing works
The Gut Microbiome–Brain Crosstalk in Neurodegenerative Diseases
Ghezzi, L., Cantoni, C., Rotondo, E., & Galimberti, D. (2022) · Biomedicines · doi:10.3390/biomedicines10071486 · Cited by 57 · see citing works
“The main symptoms of PD are resting tremors, stiffness, bradykinesia, and postural instability [80].”
BackgroundJellinger, K. A. (2019) · Journal of Neural Transmission · doi:10.1007/s00702-019-02028-6 · Cited by 55 · see citing works
Cardiac Changes in Parkinson’s Disease: Lessons from Clinical and Experimental Evidence
Cuenca‐Bermejo, L., Almela, P., Navarro‐Zaragoza, J., Fernández‐Villalba, E., Cuello, A. M. G., Laorden, M. L., & Herrero, M. T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222413488 · Cited by 53 · see citing works
“Developed more than 50 years ago, this definition based on the motor condition is no longer an accurate description for PD; numerous works have evidenced that clinical manifestations of the disease go beyond the motor system and set up a complex scenario in which non-motor symptoms appear even years before the motor o…”
Background
- Authors
- Obeso, J. A., Stamelou, M., Goetz, C. G., Poewe, W., Lang, A. E., Weintraub, D., Burn, D., Halliday, G. M., Bezard, E., Przedborski, S., Lehericy, S., Brooks, D. J., Rothwell, J. C., Hallett, M., DeLong, M. R., Marras, C., Tanner, C. M., Ross, G. W., Langston, J. W., Klein, C., Bonifati, V., Jankovic, J., Lozano, A. M., Deuschl, G., Bergman, H., Tolosa, E., Rodriguez‐Violante, M., Fahn, S., Postuma, R. B., Berg, D., Marek, K., Standaert, D. G., Surmeier, D. J., Olanow, C. W., Kordower, J. H., Calabresi, P., Schapira, A. H. V., & Stoessl, A. J.
- Affiliations
- Universidad San Pablo CEU (ES)
- Philipps University of Marburg (DE)
- Rush University Medical Center (US)
- Innsbruck Medical University (AT)
- University of Toronto (CA)
- Mental Illness Research, Education and Clinical Centers (US)
- Newcastle University (GB)
- The University of Sydney (AU)
- Université de Bordeaux Institut des Maladies Neurodégénératives, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5293, Institut des Maladies Neurodégénératives Bordeaux France
- Columbia University Irving Medical Center (US)
- Institut du Cerveau et de la Moelle épinière – ICM, Centre de NeuroImagerie de Recherche – CENIR Sorbonne Universités UPMC Univ Paris 06, Inserm U1127, CNRS UMR 7225 Paris France
- Aarhus University (DK)
- UCL Queen Square Institute of Neurology (GB)
- National Institutes of Health (US)
- Emory University (US)
- San Francisco VA Medical Center (US)
- VA Pacific Islands Health Care System (US)
- Parkinson's Institute and Clinical Center (US)
- University of Lübeck (DE)
- Erasmus MC (NL)
- Baylor College of Medicine (US)
- Christian-Albrechts-Universität zu Kiel (DE)
- Hebrew University of Jerusalem (IL)
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- Movement Disorders Clinic Clinical Neurodegenerative Research Unit Mexico City Mexico
- Montreal General Hospital (CA)
- Institute for Neurodegenerative Disorders (US)
- University of Alabama at Birmingham (US)
- Northwestern University (US)
- Icahn School of Medicine at Mount Sinai (US)
- University of Perugia (IT)
- Vancouver Coastal Health (CA)
- Corresponding author
- Obeso, J.A.
- ORCID
- Obeso, J.A.
- Stamelou, M.
- Goetz, C.G.
- Poewe, W.
- Lang, A.E.
- Weintraub, D.
- Burn, D.
- Halliday, G.M.
- Przedborski, S.
- Brooks, D.J.
- Rothwell, J.C.
- Hallett, M.
- DeLong, M.R.
- Marras, C.
- Tanner, C.M.
- Klein, C.
- Bonifati, V.
- Jankovic, J.
- Lozano, A.M.
- Deuschl, G.
- Bergman, H.
- Tolosa, E.
- Rodriguez‐Violante, M.
- Postuma, R.B.
- Berg, D.
- Marek, K.
- Standaert, D.G.
- Surmeier, D.J.
- Olanow, C.W.
- Kordower, J.H.
- Calabresi, P.
- Schapira, A.H.V.
- Stoessl, A.J.
- Venue
- Movement Disorders
- Publisher
- Wiley
- Published
- 2017-09
- Volume
- 32
- Issue
- 9
- Pages
- 1264-1310
- ISSN
- 0885-3185 (ISSN-L)
- 1531-8257
- PMC
- PMC5685546
- OpenAlex
- W2753051298
- Cited by
- 859
- References
- 308
- Citations by year
- 2026: 78 · 2025: 88 · 2024: 90 · 2023: 116 · 2022: 115 · 2021: 128 · 2020: 104 · 2019: 82 · 2018: 50 · 2017: 6 · 2015: 1
- FWCI
- 8.79
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Movement Disorders (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- National Institute of Neurological Disorders and Stroke (P50NS053488, R01NS034696)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neurology and Historical Studies
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- Parkinson's disease, history of Parkinson's disease, James Parkinson, etiopathogenesis, pathophysiology, symptomatic treatment, disease progression, future research directions
- MeSH terms
- Anniversaries and Special Events, Humans, Parkinson Disease, History, 19th Century, History, 20th Century, History, 21st Century
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